It’s not just about feeling hungry and reaching for a snack. It can also change the immune system.
Recent studies in mice have found that recognition of hunger can only change the number of immune cells in the blood even if the animal is not actually fasting. This shows that even the interpretation of hunger in the brain can shape how the immune system adapts.
New research published in Scientific Immunology Immunity challenges the longstanding idea that immunity is shaped by actual physical changes in nutrition, such as changes in blood sugar levels and changes in nutritional levels. Instead, it shows that only perception (what the brain is “thinking” is happening) can change immunity.
We focused on two types of highly specialized brain cells (AGRP and POMC neurons) It senses the state of energy in the body and produces hunger and bloating accordingly. AGRP neurons promote hunger when the energy is low, while POMC neurons show bloating after eating.
Using genetic tools, we artificially activated hanger neurons in mice that had already eaten a lot of food. Activating this small but powerful group of brain cells caused the intense urge to seek food in mice. What is this finding based on? Several previous studies have been shown.
Surprisingly, however, this synthetic starvation also led to a significant reduction in certain immune cells in the blood, called monocytes. These cells are part of the first line of defense of the immune system; Important role in the regulation of inflammation.
Conversely, when fasting mice activated filling neurons, monocyte levels approached normal, even when the mice were not eating.
These experiments showed that the brain’s perception of being hungry or being fed is itself sufficient to affect the number of immune cells in the blood.
To understand how this axis between the brain and the immune system works, we looked into how the brain communicates with the liver. This organ is important in sensing energy levels in the body. the study It also shows that the liver communicates with the bone marrow – soft tissue in the bone Blood and immune cells are produced.
We found a direct link between starvation neurons and the liver through the sympathetic nervous system. It plays a wide range of roles in regulating functions such as heart rate, blood flow, and organ responses to stress and energy demands. When hanger neurons were turned on, they dialed down liver nutrition sensing by reducing sympathetic activity.
This suggests that the brain can affect how the liver interprets the body’s energy state. We are essentially confident that even if the actual nutritional levels are normal, the energy is low. This led to a decline in chemicals, in turn, called CCL2usually helps to draw monocytes into the blood. Low CCL2 meant that there were fewer monocytes circulating.
It was also seen that hunger signals caused the release of a stress hormone called corticosterone (similar to human cortisol). This hormone itself had no significant effect on immune cell counts, at least at the level released during fasting.
Usually, much higher levels of stress hormones are required to directly affect the immune system. However, in this case, a moderate rise in corticosterone worked like an amplifier. Although it was not enough to trigger an immune change alone, it was important that the reactions occur when collaborating with signals coming from the brain.
This further shows how changes in the body’s stress system and immune system are scalable and how they can be adjusted according to the nature and intensity of stressful events.
Why does this happen?
Why does the brain do this? We haven’t officially tested this, but we believe that one possibility is that this complex, multi-organ communication system will evolve to help the body predict and respond to potential shortages. The use of fine-tuning energy based on perceived needs and immune preparation allows the brain to regulate efficient systemic responses before the actual crisis begins.
If the brain feels that food may be restricted (for example, by interpreting previously related environmental cues to food shortages), it may act early to save energy and regulate immune function in advance.
If these findings are confirmed in humans, this new data could have a real impact on diseases in which the immune system is overactive in the future. Cardiovascular disease, Multiple sclerosisand waste syndrome Cancer patients.
This is further related to metabolic disorders and eating disorders. obesity or Loss of appetite. These disorders often involve chronic inflammation and immune-related complications, but how can they be altered Hunger and fulfillment It is calculated by the brain.
And if the brain can help dial the immune system up and down, it may be possible to develop new brain targeting approaches to support current immunomodulatory therapies.
Still, there are many things we don’t know. Research is needed to investigate how this mechanism works in humans. These studies may prove challenging as it is still not possible to selectively activate specific neurons in the human brain with the accuracy that can be achieved in experimental models.
Interestingly, more than a century ago, Soviet psychiatrist A. Tapilsky used hypnosis to carry out an unusual experiment that suggested hunger and bloating towards the patient. Surprisingly, the immune cell count increased when the patient was told it was full and decreased when it was said to be hungry.
These early observations suggest a powerful mind-body connection that is far ahead of today’s scientific understanding, eerie predicting the current ability to artificially generate internal sensations such as hunger and bloating in animal models using powerful genetic tools.
What is clear is that the brain’s view of the body’s energy needs can shape the immune system – sometimes even before the body itself gets caught up in it. This raises new questions about how conditions that have learned to promote inflammation and illness, and even disease, are known to be linked to stress, eating disorders, and even food deficiency.
Giuseppeda GostinoAdvanced lecturer, Diabetes Department, Endocrinology, Gastroenterology, University of Manchester and Joan Paulo AlbuquerquePostdoctoral researcher, physiology, metabolism, University of Manchester
This article has been republished conversation Under the Creative Commons license. Please read Original article.
